YME1L1 Double Nickase Plasmid (h): sc-409793-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- YME1L1 Double Nickase Plasmid (h) consists of a pair of plasmids each encoding a D10A mutated Cas9 nuclease and a target-specific 20 nt guide RNA (gRNA) designed to knockout gene expression with greater specificity than its CRISPR/Cas9 KO counterpart
- Paired gRNA sequences are offset by approximately 20 bp to allow for specific Cas9-mediated double nicking of the genomic DNA, which mimics a DSB
- One plasmid in the pair contains a puromycin-resistance gene for selection; the other plasmid in the pair contains a GFP marker to visually confirm transfection
- YME1L1 Double Nickase Plasmid (h) and YME1L1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting YME1L1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
YME1L1 Double Nickase Plasmid (h) | sc-409793-NIC | 20 µg | $410.00 |
YME1L1 encodes a mitochondrial inner membrane AAA+ ATP-dependent metalloprotease that supports mitochondrial proteostasis by degrading misfolded or excess membrane-associated proteins and regulating turnover of key respiratory chain and membrane-shaping factors. Through quality control of the inner membrane and remodeling of protein complexes, YME1L1 contributes to oxidative phosphorylation efficiency, mitochondrial dynamics, and stress-responsive signaling pathways linked to bioenergetic homeostasis. Disruption of YME1L1 function has been associated with mitochondrial dysfunction phenotypes, including altered cristae architecture, impaired respiration, and heightened sensitivity to proteotoxic stress. These features make YME1L1 a relevant target for studying mechanisms underlying mitochondrial maintenance and pathways implicated in neurodegeneration and other mitochondria-linked disorders.
YME1L1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the YME1L1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within YME1L1. When directed to adjacent sites on opposite DNA strands, the two nickases generate offset single-strand nicks that together produce a staggered double-strand break, requiring coordinated on-target activity from both guides. The resulting DNA break is resolved by endogenous cellular repair pathways, most commonly through non-homologous end joining (NHEJ), leading to insertions or deletions that disrupt YME1L1 function. By requiring dual sgRNA engagement at the target locus, the double nicking approach enhances editing specificity and provides a complementary CRISPR strategy for applications where additional control over targeting precision is desired.
To support efficient identification of edited cells, one plasmid encodes GFP for fluorescent visualization of transfected populations, while the companion plasmid carries a puromycin resistance gene for antibiotic selection. Together, these features support efficient enrichment of co-transfected populations and simplify the validation of YME1L1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.